Tuesday, January 1, 2013

A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG:

Here is the patient's previous ECG:

Here is the patient's presenting ED ECG:﻿﻿

﻿﻿There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation. Precordial ST depression may be subendocardial ischemia or posterior STEMI. How can we tell the difference? See the list below.

If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. This was indeed done:﻿﻿

Notice the limb leads have been reversed (axes of every lead are inverted!). But we are now concerned with the precordial leads. V7-V9 (labelled V4-V6) have no ST elevation.

Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS. BP was 160/100. He was given metoprolol IV which succuessfully brought his heart rate and BP down. His chest pain resolved completely, but his ECG continued to show profound ST depression. We performed a bedside echo and found a posterior wall motion abnormality.

The cath lab was activated and the patient went for immediate angiography, which showed a 95% hazy thrombotic lesion with TIMI III flow in a large first obtuse marginal (OM-1) off the circumflex. Therefore, the angiographer had time to visualized the other arteries. The RCA was chronically occluded but supplied a small area. The LAD had a 75% proximal lesion that by fractional flow reserve was hemodynamically significant. So there was 3-vessel disease, but with an acute posterior STEMI. The OM-1 was opened and stented, then the LAD was stented 3 days later.

The acute infarct-related artery was off the circumflex and the affected wall was posterior (STEMI). The posterior leads were falsely negative. See far below for data on posterior leads.

Does this matter that the posterior ECG was a false negative? If there is ST depression (as there is here), it is ACS. Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab. And even if it is STEMI, if you get it to resolved with medical therapy, then you have opened the artery without intervention and a delay is acceptable.

Some ways to differentiate subendocardial ischemia from posterior STEMI

First, you should know that when there is precordial ST
depression due to subendocardial ischemia, it is not necessarily due to
anterior wall ischemia. Data from stress testing shows that
subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in
leads II, III, aVF and V4-V6. But, again, this does not tell you which
artery is involved. Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia. Third, patients at higher risk of NSTEMI (older, more risk
factors, h/o angiogram with multivessel disease) are much more likely
to have subendocardial disease (vs. younger smoker). Fourth, patients with reasons to have demand ischemia
(tachycardia, sepsis, GI Bleed, etc.) are much more likely to have
subendocardial ischemia (like in a stress test); those with posterior MI
are much more likely to present with onset of chest pain and with
normal vital signs. Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations). Sixth, placement of posterior leads (take leads V4-V6 and
place them at the level of the tip of the scapula, with V4 placed at the
posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5
("V8") between them. At lease 0.5 mm of ST elevation in just one lead is
very sensitive and specific for posterior MI.Seventh, an immediate echocardiogram can make the distinction. These are very difficult and it is very hard to detect a posterior wall motion abnormality unless you are very experienced. I recommend a formal study with Definity before concluding there is no posterior wall motion abnormality.Eighth, see above. Whether or not it is STEMI, the cath lab should be activated if the ischemia cannot be controlled medically: aspirin, nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor.

Here is a short summary of data on posterior leads, from:

Critical Decisions in Emergency and Acute Care Electrocardiography.William Brady and JD Truwit, editors.Blackwell Publishing 2009. (Smith SW as editor of section on Acute
Coronary Syndromes).This is a quoted excerpt from a chapter that was
written by Daniel T. O’laughlin, MD, and edited by me.

Posterior Lead Orientation and
Diagnostic Criterion

The
posterior precordial leads are positioned in the 5th intercostal
space at the same horizontal line as V6.Lead V7 is placed at the posterior axillary line, V8 just below the tip
of the scapula and V9 at the paravertebral border.1STE up to 0.5mm measured at the J point relative to the PR segment in
all three leads can be normal.2Wung and Drew evaluated the posterior ST segment changes during PTCA of
the LCX and determined that utilizing a criterion of STE of greater than or equal to 0.5mm, rather than greater than or equal to 1mm, demonstrated a sensitivity of 94% for detecting LCX occlusion related STE.3This is compared to a sensitivity of 49% when the criterion was greater than or equal to 1mm STE.Conversely, Matetzky et al. showed 100%
specificity for posterior MI of STE greater than or equal to 0.5mm in at least one posterior lead.In Wung’s study, 81% of patients with greater than or equal to 1mm
STE in posterior leads also had other significant STE on the 12-lead ECG, and
96% had some ST deviation.3 However, 22-39% of patients experiencing
posterior MI who have greater than or equal to 0.5mm STE in the posterior leads do not demonstrate STD
in V1-V3.3-5

1.Kligfield
P, Gettes LS, Bailey JJ, et al. Recommendations for the Standardization and
Interpretation of the Electrocardiogram: Part I: The Electrocardiogram and Its
Technology: A Scientific Statement From the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology;
the American College of Cardiology Foundation; and the Heart Rhythm Society
Endorsed by the International Society for Computerized Electrocardiology.
Circulation 2007;115(10):1306-24.

Disclaimer

Disclaimer: Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center

Smith-Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block

The equation for differentiating the ST elevation (STE) of subtle LAD occlusion from early repol

It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. Thus, there must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.

--QTc is the computer measurement.

--RAV4 = R-wave amplitude, in mm, in lead V4.

--ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters.